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CPR- my cards > Pathology > Flashcards

Pathology Flashcards

1
Q

Increase in pressure in the heart lead to this:

A

Pressure-overload hypertrophy

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2
Q

Pressure overload hypertrophy is manifest by:

A

concentric increase in ventricular wall thickness

- new sarcomeres parallel to old ones (stacked like paper in a notebook)

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3
Q

Excess volume affects the heart by:

A

Volume overload hypertrophy

- ventricular dilation

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4
Q

How is volume-overload hypertrophy manifest?

A 
ventricular dilation (wall may me more, less or same thickness)
- new sarcomeres are positioned in series with existing sarcomeres
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5
Q

How does hypertrophy change normal cardiac function?

A

Requires more O2 and other metabolites (increased workload)

- hypertrophy does not supply additional coronary capillaries (less supply)

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6
Q

Hypertrophic/Dilated Heart characteristics:

A
  • increase heart size/mass
  • increase protein synthesis
  • fibrosis
  • inadequate vasculature
  • –> leads to Cardiac dysfunction
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7
Q

Cardiac Dysfunction is characterized by:

A
  • systolic or diastolic heart failure
  • arrhythmias
  • neurohumoral stimulation
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8
Q

dyspnea

A

shortness of breath

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9
Q

orthopnea

A

dyspnea when lying down

improved by standing

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10
Q

What is stable angina?

A

imbalance of cardiac perfusion (low) compared with cardiac demand (higher)

  • during stress only: emotional excitement, exercise…
  • relieved by rest
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11
Q

What drug can treat stable angina?

A

nitroglycerin

- strong vasodilator that increases perfusion

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12
Q

What is prinzmetal angina?

A

coronary artery spasm causes periodic myocardial ischemia

- unrelated to physical activity, HR, or BP

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13
Q

What drugs treat prinzmetal angina?

A

Vasodilators: nitroglycerin, Ca++ channel blockers

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14
Q

What is unstable angina?

A

Increasingly frequent pain of prolonged duration that occurs even at rest (unlike stable angina)

  • usually due to disrupted atherosclerotic plaque with mural thrombosis (possibly embolism or vasospasm)
  • preinfarction angina
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15
Q 
What are the gross morphological changes due to MI at:
- 4 hours
- 24 hours
- 1 week
- 2 weeks
- 1 month
> 2months
A

4 hours: no gross features
24 hours: dark mottling (blood spots, bruise)
1 week: yellow-tan softening; hyperemic, red borders
2 weeks: red-gray depressed infarct borders
1 month: gray-white scar, outside moving to core
>2 months: scar complete, can no longer age

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16
Q 
What are the histological features due to MI at:
- 4 hours
- 24 hours
- 1 week
- 2 weeks
- 1 month
> 2 months
A

4 hours: none, possible wavy fibers of early coagulation necrosis
24 hours: coagulation necrosis, myocyte hypereosinophilia, contraction band necrosis, early neutrophils
1 week: macrophage infiltrate, phagocytize dead cells
2 weeks: granulation tissue
1 month: increased collagen deposition

17
Q

What happens to the heart in hypertrophic cardiomyopathy?

A
  • thick walled, poorly compliant L ventricle
  • septum thicker than outer wall (3:1)
  • usually without dilation
  • hypercontracting
  • diastolic dysfunction (reduced filling –> low stroke volume)
18
Q

Histologic features of HCM

Hypertrophic Cardiomyopathy

A
  • myocyte hypertrophy
  • haphazard disarray of contractile elements (myofiber disarray)
  • fibrous replacement of myocytes in ventricular wall
19
Q

Treatment for HCM

A
  • Beta blockers: decrease contractility, HR
20
Q

Clinical course/complications of HCM

A

variable
-most patients asymptomatic:
- atrial fibrillation, mural thrombus (embolization and stroke), cardiac failure, ventricular arrhythmias, sudden cardiac death
may have mitral valve prolapse/insufficiency due to high contractility an pressure of ventricle

21
Q

Gene mutations in HCM are:

A

code for sarcomere proteins

  • B-myosin heavy chain
  • cardiac troponin-T
  • myosin binding protein C
  • alpha-topomyosin
22
Q

What is DCM?

A

Dilated Cardiomyopathy

  • progressive cardiac dilation
  • systolic dysfunction (contraction)
23
Q

What is HCM?

A

Hypertrophic Cardiomyopathy

  • thickened ventricular wall due to myocyte hypertrophy
  • diastolic dysfunction (trouble relaxing)
  • decreased compliance/diastolic filling
24
Q

What causes DCM?

A
  • sometimes genetic
  • myocarditis
  • alcohol/chemo toxicity
  • peri-partum
25
Q

How does alcohol affect the heart?

A

Metabolism to acetaldehyde–> toxic to myocardium

Thiamine deficiency –> beriberi heart disease

26
Q

Clinical course of DCM:

A

slowly progressive
- dyspnea, easy fatigability, poor exertional capacity
- markedly decreased ejection fraction
- mural thrombus formation –> poss.embolism
2*: mitral regurgitation, arrhythmia

27
Q

What is amyloidosis?

A

deposition of abnormal substance in the heart

  • eosinophilic deposits surround cardiac myocytes and capillaries
  • shows apple green birefringence under polarized light with congo red stain
28
Q

Causes of fibrinous pericarditis

A 
acute MI
postinfarction Dressler syndrome
uremia
chest radiation
rheumatic fever
SLE
trauma
29
Q

What is characteristic of fibrinous pericarditis?

A

loud pericardial friction rub

pain, systemic fever suggest CF present as well

30
Q

Acute infective endocarditis differs from subacute IE in that:

A

Acute: normal heart valve and highly virulent pathogen
Subacute: abnormal heart valve and less virulent pathogen

31
Q

Most common pathogen for subacute IE:

A

Streptococcus viridans

normal oral flora

32
Q

Common pathogen for IE affecting already damaged heart valves:

A

Staph aureus

33
Q

Pathogen responsible for IE in IV drug users:

A

S. aureus

34
Q

HACEK bacteria are:

A 
bacteria of the normal oral flora
Haemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella
35
Q

Pathogen responsible for IE infection of prosthetic heart valves

A

Coagulase neg Staphylococcus

S. epidermidis

CPR- my cards (4 decks)

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